The effect of lymphatic blockage on the amount of endotoxin in portal circulation, nitric oxide synthesis, and the liver in dogs with peritonitis

Güler O., Uǧraş S., Aydin M., Dilek F. H., Dilek O. N., Karaayvaz M.

Surgery Today, vol.29, no.8, pp.735-740, 1999 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 29 Issue: 8
  • Publication Date: 1999
  • Doi Number: 10.1007/bf02482318
  • Journal Name: Surgery Today
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.735-740
  • Keywords: Endotoxin, Hepatic damage, Nitric oxide, Peritonitis
  • Çanakkale Onsekiz Mart University Affiliated: No


This study was performed to investigate the effect of lymphatic blockage on the amount of endotoxin in portal venous blood, nitric oxide synthesis, the release of aspartate aminotransferase (AST) from the liver, hepatic damage, and survival in an experimental model of dogs with peritonitis. The dogs were divided into a control group (group 1), an unligated thoracic duct peritonitis group (group 2), and a ligated thoracic duct peritonitis group (group 3). Peritoneal fluid and blood from the portal vein and femoral artery were taken for peritoneal culture, endotoxin, and AST assay, respectively, and liver biopsies were performed to assess for hepatic damage and for nitric oxide assay. There was a higher bacteria count in the peritoneal fluid from group 3 than in that from group 2 (P < 0.0001). Bacteria grew in all of the blood cultures from the group 2 animals, but growth was seen only in blood cultures from four of the group 3 animals. The levels of endotoxin, nitrite, and AST levels in group 3 were significantly increased in comparison with those in group 2 (P < 0.0001). Extensive hepatocellular necrosis with hemorrhage was observed in the livers of the group 3 animals, and all of them died within 48 h. The results of this study suggest that the blockage of lymph flow has a negative effect on liver and survival in dogs with peritonitis, and that hepatic damage is directly related to the amount of endotoxin to which the liver is exposed.